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Goodpasture syndrome is an autoimmune disease caused by antibodies against the glomerular and alveolar basement membrane. It presents with rapidly progressive glomerulonephritis (hematuria, RBC casts, renal failure) and pulmonary hemorrhage (hemoptysis, dyspnea). IgA nephropathy causes recurrent hematuria during infections but no pulmonary symptoms. Alport syndrome is a hereditary collagen disorder with hematuria, hearing loss, and ocular abnormalities. Granulomatosis with polyangiitis presents with sinusitis, lung nodules, and renal involvement but is associated with c-ANCA, not anti-GBM antibodies. Diagnosis of Goodpasture syndrome is confirmed with anti-GBM serology and renal biopsy showing linear IgG deposition. Treatment includes plasmapheresis, corticosteroids, and immunosuppressants.

The presentation is classic for chronic myeloid leukemia (CML): leukocytosis with left shift and basophilia, low LAP (distinguishing CML from a leukemoid reaction), splenomegaly, and the BCR-ABL1 fusion from t(9;22) (Philadelphia chromosome), which produces a constitutively active tyrosine kinase driving myeloid proliferation. First-line therapy is a BCR-ABL tyrosine kinase inhibitor (TKI) such as imatinib (or newer TKIs like dasatinib/nilotinib depending on risk and tolerance). TKIs induce high rates of hematologic, cytogenetic, and molecular remissions and are disease-modifying. Hydroxyurea can transiently reduce counts but does not target the molecular driver and is used as a temporizing measure. All-trans retinoic acid is specific to acute promyelocytic leukemia (APL; t(15;17) PML-RARα). Prednisone has no disease-modifying role in CML. Monitoring includes serial quantitative BCR-ABL transcripts to assess molecular response. TKI adherence, drug interactions (CYP3A4), and adverse effects (fluid retention, cytopenias, QT prolongation for some agents) must be considered. Allogeneic transplant is reserved for TKI-refractory disease or advanced phases (accelerated/blast crisis).

Acute angle-closure glaucoma is an ophthalmic emergency caused by sudden closure of the anterior chamber angle, preventing aqueous humor outflow. This leads to rapid intraocular pressure elevation, optic nerve damage, and permanent vision loss if untreated. Clinical features include severe ocular pain, headache, blurred vision, halos around lights, nausea/vomiting, conjunctival injection, corneal edema, and a mid-dilated, nonreactive pupil. In contrast, open-angle glaucoma is chronic, painless, and progressive, often asymptomatic until late visual field loss. Central retinal artery occlusion causes sudden, painless monocular vision loss with a cherry-red spot on the macula. Optic neuritis presents with painful vision loss and afferent pupillary defect, often associated with multiple sclerosis. Management of acute angle-closure includes immediate reduction of intraocular pressure with topical agents (timolol, apraclonidine, pilocarpine) and systemic medications (acetazolamide, IV mannitol), followed by definitive laser peripheral iridotomy. Prompt recognition is essential to prevent blindness.

Cellulitis is an acute bacterial infection of the dermis and subcutaneous tissue. Clinical features include erythema, warmth, swelling, pain, and systemic signs (fever, leukocytosis) in moderate-to-severe cases. The most common cause is β-hemolytic streptococci (particularly Streptococcus pyogenes). These organisms spread rapidly along superficial lymphatics, producing ill-defined borders. Staphylococcus aureus, especially MRSA, is more associated with purulent skin infections (abscesses, furuncles, carbuncles). Pseudomonas is seen in puncture wounds through shoes or immunocompromised patients. Candida causes cutaneous candidiasis in moist intertriginous areas, but not rapidly spreading cellulitis. Management involves systemic antibiotics (e.g., cephalexin, clindamycin, or vancomycin depending on severity and MRSA risk). Complications include bacteremia, necrotizing fasciitis, and sepsis. Distinguishing erysipelas (well-demarcated, superficial) from cellulitis (deeper, ill-defined) aids diagnosis, but both are streptococcal predominant.